Modulating Neuroinflammation as a Prospective Therapeutic Target in Alzheimer’s Disease
Cells,
Год журнала:
2025,
Номер
14(3), С. 168 - 168
Опубликована: Янв. 22, 2025
The
recent
approval
of
lecanemab
highlights
that
the
amyloid
beta
(Aβ)
protein
is
an
important
pathological
target
in
Alzheimer’s
disease
(AD)
and
further
emphasizes
significance
neuroinflammatory
pathways
regulating
Aβ
accumulation.
Indeed,
accumulation
triggers
microglia
activation,
which
are
key
mediators
neuroinflammation.
inflammatory
responses
this
process
can
lead
to
neuronal
damage
functional
decline.
Microglia
secrete
proinflammatory
cytokines
accelerate
death
release
anti-inflammatory
growth
factors
contributing
recovery
protection.
Thus,
play
a
dual
role
neurodegeneration
neuroprotection,
complicating
their
function
AD.
Therefore,
elucidating
complex
interactions
between
protein,
microglia,
neuroinflammation
essential
for
developing
new
strategies
treating
This
review
investigates
receptors
involved
activating
aims
enhance
understanding
how
these
processes
impact
AD,
as
well
they
be
regulated.
also
analyzed
studies
reported
existing
literature
ongoing
clinical
trials.
Overall,
will
contribute
regulatory
mechanisms
therapies
slow
progression
Язык: Английский
Unraveling the Protective Role of Oleocanthal and Its Oxidation Product, Oleocanthalic Acid, against Neuroinflammation
Antioxidants,
Год журнала:
2024,
Номер
13(9), С. 1074 - 1074
Опубликована: Сен. 3, 2024
Neuroinflammation
is
a
critical
aspect
of
various
neurodegenerative
diseases,
such
as
Alzheimer's
and
Parkinson's
diseases.
This
study
investigates
the
anti-neuroinflammatory
properties
oleocanthal
its
oxidation
product,
oleocanthalic
acid,
using
BV-2
cell
line
activated
with
lipopolysaccharide.
Our
findings
revealed
that
significantly
inhibited
production
pro-inflammatory
cytokines
reduced
expression
inflammatory
genes,
counteracted
oxidative
stress
induced
by
lipopolysaccharide,
increased
phagocytic
activity.
Conversely,
acid
was
not
able
to
counteract
lipopolysaccharide-induced
activation.
The
docking
analysis
plausible
interaction
oleocanthal,
both
CD14
MD-2
leading
potential
interference
TLR4
signaling.
Since
our
data
show
only
partially
reduces
activation
NF-kB,
action
antagonist
alone
cannot
explain
remarkable
effect
against
neuroinflammation.
Proteomic
counteracts
LPS
modulation
31
proteins,
including
significant
targets
gelsolin,
clathrin,
ACOD1,
four
different
isoforms
14-3-3
protein,
indicating
new
molecular
compound.
In
conclusion,
but
mitigates
neuroinflammation
through
multiple
mechanisms,
highlighting
pleiotropic
particularly
important
in
context
neurodegeneration.
Язык: Английский